Modélisation du séchage convectif et symétrique des bois d’ayous, d’eucalyptus grandis et d’ébène : simulation numérique et validation expérimentale

Dans cet article, nous développons un modèle de séchage du bois en nous inspirant de la littérature. Des hypothèses sont ensuite retenues afin de simuler le comportement des bois d’ayous (Triplochiton scleroxylon), d’Eucalyptus grandis et d’ébène (Diospyros crassiflora hiern). Les coefficients thermophysiques des bois sont tirés de la littérature. Les résultats de la simulation numérique montrent que le modèle peut être utilisé pour améliorer le fonctionnement des séchoirs convectifs. On constate néanmoins un léger écart entre les points expérimentaux et les résultats de la simulation numérique. Cet écart serait la conséquence des hypothèses simplificatrices adoptées, de la prise en compte dans le programme de certains coefficients thermophysiques obtenus sur des bois autres que ceux d’étude et des erreurs enregistrées durant l’expérience ayant permis d’obtenir les cinétiques expérimentales. L’utilisation des points expérimentaux obtenus par D. Guoxing et al. (2003a, 2003b) nous permet de constater que le modèle peut aussi être utilisé pour simuler le séchage des bois tempérés de forte épaisseur (25 mm). Le bois d’ayous sèche plus vite que le bois d’ébène. En suivant la table de séchage du bois d’ayous, la durée de l’opération de séchage est réduite d’environ 20h de celle nécessaire pour mener le séchage avec une température de l’air de 40°C. On n’observe pas de modification de la durée de séchage du bois d’ébène, l’épaisseur des planches étant de 12mm et la teneur en eau initiale évaluée à 35 %. La simulation du séchage sur le bois d’eucalyptus montre que la surface sèche plus vite que l’intérieur et si le séchage n’est pas suivi, la surface est exposée au jeu retrait-gonflement qui aboutit aux fentes superficielles.Mots-clés : séchage convectif, modélisation, simulation numérique, bois, ayous, ébène, eucalyptus grandis

Modelling of the Water Absorption Kinetics and Determination of the Water Diffusion Coefficient in the Pith of Raffia vinifera

The present work focuses on the study of the water absorption phenomenon through the pith of Raffia vinifera along the stem. The water absorption kinetics was studied experimentally by the gravimetric method with the discontinuous control of the sampling mass at temperature of 30°C. The samples of 70 mm × 8 mm × 4 mm were taken from twelve sampling zones of the stem of Raffia vinifera. The result shows that the percentage of water absorption of the pith of Raffia vinifera increases from the periphery to the center in the radial position and from the base to the leaves in the longitudinal position. Fick’s second law was adopted for the study of the water diffusion. Eleven models were tested for the modelling of the water absorption kinetics and the model of Sikame Tagne (2014) is the optimal model. The diffusion coefficients of two stages were determined by the solution of the Fick equation in the twelve sampling zones described by Sikame Tagne et al. (2014). The diffusion coefficients decreased from the center to the periphery in the radial position and from the base to the leaves in the longitudinal position

NAAA-regulated lipid signaling governs the transition from acute to chronic pain

Chronic pain affects 1.5 billion people worldwide but remains woefully undertreated. Understanding the molecular events leading to its emergence is necessary to discover disease-modifying therapies. Here we show that N-acylethanolamine acid amidase (NAAA) is a critical control point in the progression to pain chronicity, which can be effectively targeted by small-molecule therapeutics that inhibit this enzyme. NAAA catalyzes the deactivating hydrolysis of palmitoylethanolamide, a lipid-derived agonist of the transcriptional regulator of cellular metabolism, peroxisome proliferator-activated receptor-α (PPAR-α). Our results show that disabling NAAA in spinal cord during a 72-h time window following peripheral tissue injury halts chronic pain development in male and female mice by triggering a PPAR-α-dependent reprogramming of local core metabolism from aerobic glycolysis, which is transiently enhanced after end-organ damage, to mitochondrial respiration. The results identify NAAA as a crucial control node in the transition to chronic pain and a molecular target for disease-modifying medicines

Transcription factor and microRNA interactions in lung cells: an inhibitory link between NK2 homeobox 1, miR-200c and the developmental and oncogenic factors Nfib and Myb

Background: The transcription factor NK2 homeobox 1 (Nkx2-1) plays essential roles in epithelial cell proliferation and differentiation in mouse and human lung development and tumorigenesis. A better understanding of genes and pathways downstream of Nkx2-1 will clarify the multiple roles of this critical lung factor. Nkx2-1 regulates directly or indirectly numerous protein-coding genes; however, there is a paucity of information about Nkx2-1-regulated microRNAs (miRNAs). Methods and results: By miRNA array analyses of mouse epithelial cell lines in which endogenous Nkx2-1 was knocked-down, we revealed that 29 miRNAs were negatively regulated including miR-200c, and 39 miRNAs were positively regulated by Nkx2-1 including miR-1195. Mouse lungs lacking functional phosphorylated Nkx2-1 showed increased expression of miR-200c and alterations in the expression of other top regulated miRNAs. Moreover, chromatin immunoprecipitation assays showed binding of NKX2-1 protein to regulatory regions of these miRNAs. Promoter reporter assays indicated that 1kb of the miR-200c 5′ flanking region was transcriptionally active but did not mediate Nkx2-1- repression of miR-200c expression. 3′UTR reporter assays support a direct regulation of the predicted targets Nfib and Myb by miR-200c. Conclusions: These studies suggest that Nkx2-1 controls the expression of specific miRNAs in lung epithelial cells. In particular, we identified a regulatory link between Nkx2-1, the known tumor suppressor miR-200c, and the developmental and oncogenic transcription factors Nfib and Myb, adding new players to the regulatory mechanisms driven by Nkx2-1 in lung epithelial cells that may have implications in lung development and tumorigenesis. Keywords: microRNA Transcription factors Gene expression Lung epithelial cells Target

Multi‐omics analysis identifies a CYP9K1 haplotype conferring pyrethroid resistance in the malaria vector Anopheles funestus in East Africa

Metabolic resistance to pyrethroids is a menace to the continued effectiveness of malaria vector controls. Its molecular basis is complex and varies geographically across Africa. Here, we used a multi-omics approach, followed-up with functional validation to show that a directionally selected haplotype of a cytochrome P450, CYP9K1 is a major driver of resistance in Anopheles funestus. A PoolSeq GWAS using mosquitoes alive and dead after permethrin exposure, from Malawi and Cameroon, detected candidate genomic regions, but lacked consistency across replicates. Targeted sequencing of candidate resistance genes detected several SNPs associated with known pyrethroid resistance QTLs. The most significant SNPs were in the cytochrome P450 CYP304B1 (Cameroon), CYP315A1 (Uganda) and the ABC transporter gene ABCG4 (Malawi). However, when comparing field resistant mosquitoes to laboratory susceptible, the pyrethroid resistance locus rp1 and SNPs around the ABC transporter ABCG4 were consistently significant, except for Uganda where SNPs in the P450 CYP9K1 was markedly significant. In vitro heterologous metabolism assays with recombinant CYP9K1 revealed that it metabolises type II pyrethroid (deltamethrin; 64% depletion) but not type I (permethrin; 0%), while moderately metabolising DDT (17%). CYP9K1 exhibited reduced genetic diversity in Uganda underlying an extensive selective sweep. Furthermore, a glycine to alanine (G454A) amino acid change in CYP9K1 was fixed in Ugandan mosquitoes but not in other An. funestus populations. This study sheds further light on the evolution of metabolic resistance in a major malaria vector by implicating more genes and variants that can be used to design field-applicable markers to better track resistance Africa-wide

Nasal Accumulation and Metabolism of Δ9-Tetrahydrocannabinol Following Aerosol (‘Vaping’) Administration in an Adolescent Rat Model

Passive aerosol exposure to Δ9-tetrahydrocannabinol (THC) in laboratory animals results in faster onset of action and less extensive liver metabolism compared to most other administration routes and might thus provide an ecologically relevant model of human cannabis inhalation. Previous studies have, however, overlooked the possibility that rodents, as obligate nose breathers, may accumulate aerosolized THC in the nasal cavity, from where the drug might directly diffuse to the brain. To test this, we administered THC (ten 5-s puffs of 100 mg/mL of THC) to adolescent (31-day-old) Sprague-Dawley rats of both sexes. We used liquid chromatography/tandem mass spectrometry to quantify the drug and its first-pass metabolites – 11-hydroxy-Δ9-THC (11-OH-THC) and 11-nor-9-carboxy-Δ9-THC (11-COOH-THC) – in nasal mucosa, lungs, plasma, and brain (olfactory bulb and cerebellum) at various time points after exposure. Apparent maximal THC concentration and area under the curve were ∼5 times higher in nasal mucosa than in lungs and 50–80 times higher than in plasma. Concentrations of 11-OH-THC were also greater in nasal mucosa and lungs than other tissues, whereas 11-COOH-THC was consistently undetectable. Experiments with microsomal preparations confirmed local metabolism of THC into 11-OH-THC (not 11-COOH-THC) in nasal mucosa and lungs. Finally, whole-body exposure to THC deposited substantial amounts of THC (∼150 mg/g) on fur but suppressed post-exposure grooming in rats of both sexes. The results indicate that THC absorption and metabolism in nasal mucosa and lungs, but probably not gastrointestinal tract, contribute to the pharmacological effects of aerosolized THC in male and female rats

Genome-Wide Analyses of Nkx2-1 Binding to Transcriptional Target Genes Uncover Novel Regulatory Patterns Conserved in Lung Development and Tumors

The homeodomain transcription factor Nkx2-1 is essential for normal lung development and homeostasis. In lung tumors, it is considered a lineage survival oncogene and prognostic factor depending on its expression levels. The target genes directly bound by Nkx2-1, that could be the primary effectors of its functions in the different cellular contexts where it is expressed, are mostly unknown. In embryonic day 11.5 (E11.5) mouse lung, epithelial cells expressing Nkx2-1 are predominantly expanding, and in E19.5 prenatal lungs, Nkx2-1-expressing cells are predominantly differentiating in preparation for birth. To evaluate Nkx2-1 regulated networks in these two cell contexts, we analyzed genome-wide binding of Nkx2-1 to DNA regulatory regions by chromatin immunoprecipitation followed by tiling array analysis, and intersected these data to expression data sets. We further determined expression patterns of Nkx2-1 developmental target genes in human lung tumors and correlated their expression levels to that of endogenous NKX2-1. In these studies we uncovered differential Nkx2-1 regulated networks in early and late lung development, and a direct function of Nkx2-1 in regulation of the cell cycle by controlling the expression of proliferation-related genes. New targets, validated in Nkx2-1 shRNA transduced cell lines, include E2f3, Cyclin B1, Cyclin B2, and c-Met. Expression levels of Nkx2-1 direct target genes identified in mouse development significantly correlate or anti-correlate to the levels of endogenous NKX2-1 in a dosage-dependent manner in multiple human lung tumor expression data sets, supporting alternative roles for Nkx2-1 as a transcriptional activator or repressor, and direct regulator of cell cycle progression in development and tumors

Radiative heat transfer using isotropic scaling approximation : application to fibrous medium

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